The objective of this proposal is to test the hypothesis that SIDS is caused by obstructive sleep apnea (OSA). This hypothesis is based on the fact that at autopsy of SIDS victims, there are intrathoracic petechiae, pulmonary edema, and hypertrophy of diaphragmatic muscle fibers, as well as markers of chronic hypoxia. All these findings are best explained by repetitive episodes of obstructive apnea. The anatomically crowded upper airway in infancy is very vulnerable to obstruction, and the infant medulla gliosis found in SIDS victims involves nuclei crucial to the control of breathing, which eventually disrupts the ventilatory and arousal responses to asphyxia, thereby turning a simple apnea into a lethal event. We have recently developed a canine model of OSA. The model consists of adult dogs that breathe through an endotracheal tube inserted through a chronic tracheostomy. The EEG and nuchal EMG are monitored continuously and are sent by telemetry to a computer that has been programmed to recognize sleep and arousals. At a chosen interval after sleep onset, the computer generates a signal that is sent by an FM transmitter, causing a valve to occlude the endotracheal tube. Obstruction continues until EEG/EMG arousal is detected, and the valve occlusion is released. When the next sleep onset is detected, the sequence is repeated. We propose to modify this system for use in the newborn puppy, so that the rate of development of the syndrome can be regulated over a 120 day schedule (equivalent to the first year of life of the human infant). Information will be collected regarding the time course, sequence, and extent of changes in respiratory drive, arterial 02 saturation, heart rate, and arousal responses to airway occlusion, with particular attention to potential physiological markers of SIDS. After 120 days the animals will be sacrificed to determine if the pathological changes in this model replicate those in SIDS.